A guide for endometrial cancer cell lines functional assays using the measurements of electronic impedance

Kozak, Joanna; Wdowiak, Paulina; Maciejewski, Ryszard; Torres, Anna

doi:10.1007/s10616-017-0149-5

Cited by 28 publications

(20 citation statements)

References 25 publications

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“…Some of our subtype classification results are consistent with prior observations. For example, HEC-1A, HEC-1B, and KLE were previously characterized as type II endometrial cancer, which includes a serous histological subtype 55 . On the other hand, our subtype classification results contradict prior observations in at least one case.…”

Section: Resultsmentioning

confidence: 99%

“…On the other hand, our subtype classification results contradict prior observations in at least one case. For instance, the Ishikawa cell line was derived from type I endometrial cancer (endometrioid histological subtype) 55,56 , however CCN classified a derivative of this line, Ishikawa 02 ER-, as serous. The high serous CCN score could result from a shift in phenotype of the line concomitant with its loss of estrogen receptor (ER) as this is a distinguishing feature of type II endometrial cancer (serous histological subtype) 52 .…”

Section: Resultsmentioning

confidence: 99%

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Evaluating the transcriptional fidelity of cancer models

Peng

Gleyzer

Tai

et al. 2020

Preprint

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33 34 35 * These authors made equal contributions. 36 37 38 Correspondence to: patrick.cahan@jhmi.edu 39 40 Article type: Analysis 41 42 Website: http://www.cahanlab.org/resources/cancerCellNet_web 43 44 Code: https://github.com/pcahan1/cancerCellNet 45 46 47 48 49 2 ABSTRACT 50 51Cancer researchers use cell lines, patient derived xenografts, and genetically engineered mice 52 as models to investigate tumor biology and to identify therapies. The generalizability and power 53 of a model derives from the fidelity with which it represents the tumor type of investigation, 54 however, the extent to which this is true is often unclear. The preponderance of models and the 55 ability to readily generate new ones has created a demand for tools that can measure the extent 56 and ways in which cancer models resemble or diverge from native tumors. Here, we present a 57 computational tool, CancerCellNet, that measures the similarity of cancer models to 22 naturally 58 occurring tumor types and 36 subtypes, in a platform and species agnostic manner. We applied 59 this tool to 657 cancer cell lines, 415 patient derived xenografts, and 26 distinct genetically 60 engineered mouse models, documenting the most faithful models, identifying cancers 61 underserved by adequate models, and finding models with annotations that do not match their 62 classification. By comparing models across modalities, we find that genetically engineered mice 63 have higher transcriptional fidelity than patient derived xenografts and cell lines in four out of 64 five tumor types. We have made CancerCellNet available as freely downloadable software and 65 as a web application that can be applied to new cancer models. 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81Models are widely used to investigate cancer biology and to identify potential therapeutics. 82Popular modeling modalities are cancer cell lines (CCLs) 1 , genetically engineered mouse 83 models (GEMMs) 2 , and patient derived xenografts (PDXs) 3 .These classes of models differ in the 84 types of questions that they are designed to address. CCLs are often used to address cell 85 intrinsic mechanistic questions 4 , GEMMs to chart progression of molecularly defined-disease 5 , 86 and PDXs to explore patient-specific response to therapy in a physiologically relevant context 6 . 87Models also differ in the extent to which the they represent specific aspects of a cancer type 7 . 88Even with this intra-and inter-class model variation, all models should represent the tumor type 89 or subtype under investigation, and not another type of tumor, and not a non-cancerous tissue. 90Therefore, cancer-models should be selected not only based on the specific biological question 91 but also based on the similarity of the model to the cancer type under investigation 8,9 . 92 Various methods have been proposed to determine the similarity of cancer models to 93 their intended subjects. Domcke et al devised a 'suitability score' as a metric of the molecular 94 similarity of CCLs to high grade serous ovarian carcinom...

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Evaluating the transcriptional fidelity of cancer models

Peng

Gleyzer

Tai

et al. 2020

Preprint

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“…Our study is the first to show that the antioxidant protein SESN1 is not expressed in any of the analyzed EC cell lines. The expression of SESN2 protein in AN3CA cells, which were derived from undifferentiated metastatic endometrial adenocarcinoma, classified as poorly differentiated grade 3 (G3), estrogen (ER), and progesterone receptors (PR) positive type II EC [35], was higher than that in Ishikawa cells, which were derived from well-differentiated G1, type I endometrial adenocarcinoma [35]. Moreover, we observed strong expression of SESN2 protein in RL-92-5 cells derived from a moderately differentiated G2 endometrial adenosquamous carcinoma representing type I [36].…”

Section: Discussionmentioning

confidence: 99%

Interactions between microRNA-200 family and Sestrin proteins in endometrial cancer cell lines and their significance to anoikis

et al. 2019

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In the present study, we intend to determine whether Sestrin proteins 1, 2, and 3 (SESN1-3) are targets of microRNA-200 family (miR-200) in endometrial cancer (EC) Ishikawa, AN3CA, KLE, and RL 95-2 cell lines and to investigate how these potential interactions influence anoikis resistance of EC cell lines. The luciferase reporter assay, qRT-PCR, and western blotting assays were used to verify whether SESN1-3 are direct targets of miR-200. Moreover, the anoikis assay and transient transfections of miR-200 mimics or inhibitors into EC cell lines were performed to evaluate the modulatory role of miR-200 and SESN proteins on anoikis resistance. We demonstrated that SESN2 protein is a direct target of mir-141 in KLE and RL-95-2 EC cell lines and the functional interaction of miR-141 and SESN2 protein has a downstream effect on anoikis resistance and SESN2 expression level in Ishikawa and AN3CA cell lines. Moreover, we have shown that SESN3 protein is a direct target of miR-200b, miR-200c, and miR-429 in Ishikawa, AN3CA, and KLE cell lines. Our results show that manipulation of miR-200b, miR-200c, and miR-429 expression patterns also has an influence on anoikis resistance in EC cell lines. In conclusion, we identified new interactions between miR-200 and the oxidative stress response SESN proteins that affect anoikis resistance in human EC cells.

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“…In addition, in subsequent analyses, it would be reasonable to determine the effect of salinomycin on the induction of apoptosis in normal endometrial cells, since the main premise of anti-cancer therapies is the activation of apoptosis only in tumor cells [ 40 ] and in other endometrial cancer cell lines, i.e . HEC-1-A, HEC-1-B and KLE [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Effect of Salinomycin on Expression Pattern of Genes Associated with Apoptosis in Endometrial Cancer Cell Line

Kiełbasiński

Peszek²,

Grabarek³

et al. 2020

CPB

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Background:: Salinomycin is part of a group of ionophore antibiotics characterized by an activity towards tumor cells. To this day, the mechanism through which salinomycin induces their apoptosis is not fully known yet. The goal of this study was to assess the expression pattern of genes and the proteins coded by them connected with the process of programmed cell death in an endometrial cancer cell Ishikawa culture exposed to salinomycin and compared to the control. Material and methods: Analysis of the effect of salinomycin on Ishikawa endometrial cancer cells (ECACC 99040201) included a cytotoxicity MTT test (with a concentration range of 0.1-100 µM), assessment of the induction of apoptosis and necrosis by salinomycin at a concentration of 1 µM as well the assessment of the expression of the genes chosen in the microarray experiment (microarray HG-U 133A_2) and the proteins coded by them connected with apoptosis (RTqPCR, ELISA assay). The statistical significance level for all analyses carried out as part of this study was p<0.05. Results: It was observed that salinomycin causes the death of about 50% of cells treated by it(50.74±0.80 % of all cells) at a concentration of 1µM. The decrease in the number of living cells was determined directly after treatment of the cells with the drug (time 0). The average percent of late apoptotic cells was 1.65±0.24% and 0.57±0.01% for necrotic cells throughout the entire observation period. Microarray analysis indicated the following number of mRNA differentiating the culture depending on the time of incubation with the drug: H_12 vs C = 114 mRNA, H_8 vs C = 84 mRNA, H_48 vs C = 27 mRNA, whereas 5 mRNA were expressed differently at all times. During the whole incubation period of the cells with the drug, the following dependence of the expression profile of the analyzed transcripts was observed: Bax>p53>FASL>BIRC5>BCL2L. Conclusions: The analysis that was carried out indicated that salinomycin, at a concentration of 1 µM, stops the proliferation of 50% of endometrial cancer cells, mainly by inducing the apoptosis process of the cells. The molecular exponent of the induction of programmed cell death was an observed increase in the transcriptional activity of pro-apoptotic genes: Bax;p53;FASL and a decrease in the expression of anti-apoptotic genes: BCL2L2; BIRC5.

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A guide for endometrial cancer cell lines functional assays using the measurements of electronic impedance

Cited by 28 publications

References 25 publications

Evaluating the transcriptional fidelity of cancer models

Evaluating the transcriptional fidelity of cancer models

Interactions between microRNA-200 family and Sestrin proteins in endometrial cancer cell lines and their significance to anoikis

Effect of Salinomycin on Expression Pattern of Genes Associated with Apoptosis in Endometrial Cancer Cell Line

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